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We can reassure Taylor that the wider context of hypertension
associated with multicystic dysplastic kidney (MCDK) was not missed in
this review, for the following reasons:

1. The purpose of the review was to quantify the risk of hypertension
associated with a unilateral MCDK based on longitudinal cohort studies,
irrespective of the mechanism(s) for that hypertension, and which single
case re...

We can reassure Taylor that the wider context of hypertension
associated with multicystic dysplastic kidney (MCDK) was not missed in
this review, for the following reasons:

1. The purpose of the review was to quantify the risk of hypertension
associated with a unilateral MCDK based on longitudinal cohort studies,
irrespective of the mechanism(s) for that hypertension, and which single
case reports definitely cannot answer. We are therefore confident that all
cases, regardless of their theoretical pathophysiology for hypertension,
have been included. Interestingly, the case reports cited by Taylor seem
to invalidate his statement that the absence of renal elements in the non-
functioning MCDK makes it unlikely to be the cause of hypertension, as
most showed that nephrectomy of the dysplastic kidney led to normalisation
of the blood pressure. These simple clinical observations highlight how
much we do not know despite the numerous theories and animal experiments
extensively referenced by Taylor.

2. Taylor correctly reminds us that abnormalities in the
controlateral kidney probably increase the risk of hypertension. This is
exactly why, in an attempt to quantify the risk of a single affected
kidney, only unilateral MCKD with a radiologically normal controlateral
kidney were analysised. The number of nephrons in the radiologically
normal controlateral kidney was obviously not available in any of the
cohort studies, nor is it currently routinely sought when following up
such children. It remains therefore impossible to validate if Taylor's
statement of the number of nephrons in the controlateral kidney applies to
all children with unilateral MCDK. Again, this does not matter at all in
our review as we included all hypertensive children regardless of the
possible mechanism for hypertension.

3. We also mentioned that many cases of unilateral renal agenesis
(RA) may be due to involution of a MCDK. However, as it is impossible
retrospectively to correctly attribute each case of RA to that involution
process, we felt it was inappropriate to include all cases of RA to those
with unilateral MCDK. The theoretical effect of reduction of the number of
nephrons in unilateral RA on the risk of hypertension is certainly
important, but unilateral RA was specifically excluded in this review.

4. Taylor rightly questions the dichotomous studied outcome:
hypertension versus normal blood pressure. Unfortunately, this was how the
studied cohorts classified the outcomes, and, in the absence of specific
blood pressure measurements given for each child, that was the only
information available for analysis.

5. The study of 24-hour blood pressure monitoring mentioned by Taylor
was specifically excluded as it dealt with children with a solitary
kidney, who were excluded for the many reasons given above. In addition,
24-hour blood pressure monitoring was not available in all the selected
cohorts. We also stated that longer follow up studies are required.

6. Taylor also implies that there is already information on that
outcome. Unfortunately, it takes more than case reports and experimental
animal data to provide a quantitative answer to the family of a child with
MCDK : "doctor, what is the risk of my child having hypertension later in
life?", and this regardless of the possible different mechanisms
underlying their hypertension. This review, despite its limitations,
provides an estimate, albeit imperfect, of that risk, and more
importantly, shows the methods required to develop much needed better
prospective longitudinal studies, based on a national MCDK registry and
using stricter blood pressure measurements reporting over a much longer
period, as discussed also in the preceding 2 paragraphs.

7. We agree that BP monitoring in adulthood is required, but not only
for these children, but also for the whole population where the risk
of hypertension of any cause is already very high. However this
recommendation, although important, still does little to provide an answer
today to the question asked by the family of a child with MCDK.
Fortunately, the systematic review, despite its many weaknesses, brings
today the answer a little bit closer.

Many thanks to Doctors Kerur and Kumar for providing the image of a
human eye with a brown deposit at the outer border of the cornea, which is
seen in Wilson disease. This clinical sign is actually known as Kayser-
Fleischer ring, not Kayser-Fischer ring as indicated in the text, and is
named after Bernhard Kayser (1869 - 1954) and Bruno Fleischer (1874 -
1965).

I was amazed to read the positive tone of the discussion in a recent
article published in your journal which concluded that supplementation
with a probiotic is beneficial in improving the extent and severity of AD
in young children (Arch Dis Child 2005;90:892-897). This was despite the
fact that the data clearly showed no significant difference in improvement
between the placebo and treatment groups....

I was amazed to read the positive tone of the discussion in a recent
article published in your journal which concluded that supplementation
with a probiotic is beneficial in improving the extent and severity of AD
in young children (Arch Dis Child 2005;90:892-897). This was despite the
fact that the data clearly showed no significant difference in improvement
between the placebo and treatment groups. The result that was discussed at
length was the significant difference before and after probiotics without
taking into account the placebo group. Why construct such a careful
randomised double blind placebo controlled trial and then completely
disregard the control group when drawing conclusions? I could find no
support for the editorial statement that "probiotics may indeed provide
benefit in infant eczema" from this study.

The power of a systematic review is only as good as the question
being posed. In his review of the risk of hypertension in children with
multicystic kidney disease (MCKD), Narchi misses the wider context.[1]
There may be more than one relationship between the diagnosis of MCKD and
blood pressure (BP). Perhaps the component in the mind of the author is
that a multicystic dysplastic kidney might in itse...

The power of a systematic review is only as good as the question
being posed. In his review of the risk of hypertension in children with
multicystic kidney disease (MCKD), Narchi misses the wider context.[1]
There may be more than one relationship between the diagnosis of MCKD and
blood pressure (BP). Perhaps the component in the mind of the author is
that a multicystic dysplastic kidney might in itself be a cause of
hypertension. This seems unlikely if the affected kidney is non-
functioning and contains no renal elements. His review supports this
presumption, although exceptions are clearly reported.[2] The majority of
non-functioning multicystic dysplastic kidneys involute, so that a
proportion of individuals who had MCKD originally are diagnosed later as
having unilateral renal agenesis (RA), technically a misnomer in this
case. It would make more sense to widen the enquiry to include this
category.

An important consideration is the role of the contralateral kidney in
the regulation of BP in these patients. Firstly, the contralateral kidney
will prove to be radiologically abnormal in about a quarter of cases of
MCKD or RA. Coarse focal scarring, hydronephrosis or hypoplasia would be
expected to have an impact on BP depending on the nature of the
abnormality.

Radiologically normal solitary kidneys can also predispose to
hypertension. Although they are significantly larger than normal paired
kidneys and their complement of nephrons is unknown, there are good
reasons to consider that patients with MCKD or RA embark upon life with a
reduced number of nephrons. There are data to indicate that a modest
reduction in the number of nephrons, even in people with two kidneys, is a
risk factor for the development of hypertension.[3,4] This is supported
by studies in other species, and in a variety of models.[5,6,7] For
example uni-nephrectomy in rat pups and in the ovine foetus induces salt
sensitive hypertension that takes time to evolve.

Blood pressure is a continuous variable in the population and
correlations between BP and cardiovascular disease extend well into the
normal range.[8] Therefore the separation of hypertension from
normotension is somewhat arbitrary, and the qualitative end point does not
serve the analysis very well, particularly in young subjects who have yet
to disclose overt hypertension however defined. A correlation with the
quantitative variable of blood pressure is more relevant. Omitted from the
review is the observation that a subtle but significant increase in BP can
be found in children with a solitary kidney using 24 hour ambulatory BP
recording.[11] Moreover, there are enough follow up studies of adults
with either unilateral RA or surgical loss of one kidney in childhood to
suggest an increase risk of hypertension even when the remaining kidney is
thought to be “normal”[9,10] It clearly takes time, certainly more than
20 years, for this end point to be reached.

Narchi’s plea for long term follow-up is a sound one but should not
be based on the premise that there is no information on outcome. On the
contrary, there is enough positive information to indicate that
individuals with MCDK, RA or renal loss for other reasons early in life
deserve BP monitoring in adulthood, especially if there are additional
risk factors such as obesity.[12]

We read with interest the recent article by Stordal et al. on acid
suppression in children in with asthma and gastro-oesophageal reflux
disease.[1] The authors concluded omeprazole treatment did not improve
asthma symptoms or lung function in children with asthma and gastro-oesophageal reflux disease.

Since Kennedy.[2] first reported the association between gastro-oesophageal reflux and lung di...

We read with interest the recent article by Stordal et al. on acid
suppression in children in with asthma and gastro-oesophageal reflux
disease.[1] The authors concluded omeprazole treatment did not improve
asthma symptoms or lung function in children with asthma and gastro-oesophageal reflux disease.

Since Kennedy.[2] first reported the association between gastro-oesophageal reflux and lung disease 43 years ago, a number of publications
have reported its’ strong association with asthma; prevalence ranging from
34% to 89%.[3] If acid suppression is really achieved in the current
study, why was there a negative result?[1] We believe there are important
potential limitations in the study.

There are concerns about the management of the study subjects. The
severity of asthma was classified as the GINA guidelines.[4] According to
the authors, 31 children had persistent asthma (steps 2 and 3) and seven
had episodic asthma. Yet, 34 patients were administered daily-inhaled
steroids (indicated for steps 2 and beyond as per GINA guidelines).
Similarly, long acting bronchodilators are indicated for use in moderate
and severe persistent asthma (steps 3 and 4). However, these drugs were
used in 22 children while there were only 17 children with moderate
persistent asthma in the study.[1] From this it appears that the study
subjects were over-treated.

To evaluate the effect of acid suppression on symptom control in
children with asthma and gastro-oesophageal reflux, it is desirable to
enrol children with asthma who have symptoms attributable to gastro-oesophageal reflux. The diagnosis of gastro-oesophageal reflux disease by
a 24-hour pH study and documentation of reflux index alone is not enough.
The quality of study may have been improved by simultaneously measurement
of proximal and distal oesophageal pH using dual probes, correlation of pH
changes with episodes of cough and asthma exacerbation, measurement of
peak expiratory flow rate and forced expiratory volume in the first second
during or immediately after a reflux episode.[5]

Authors did not enrol children with ‘difficult to control’ asthma.
In clinical practice, the important question to address is ‘whether
therapy for gastro-oesophageal reflux improves asthma symptom control in
children with difficult asthma and reflux disease? Previous studies
showed reflux is reportedly more common in poorly controlled patients than
in well-controlled patients[6,7] suggesting that reflux may be
responsible for poor control.

The duration of acid suppression was too short to show a predictable
improvement in asthma. Longer period of suppression is essential for
proper assessment of clinical parameters (i.e. changes in asthma
medication, reduction in method dosage, number of exacerbations and
seasonal variation).

In addition, it is not clear whether any anti-reflux measures were
used in the study subjects such as prokinetics and lifestyle
modifications. These may be important as preventing reflux may in itself
lead to symptom control as has been seen with surgical treatment.[8]

A major flaw in the study design, also mentioned by the authors, was
the small sample size. With such small sample size the possibility of type
II error cannot be excluded. The authors may provide more details of the
sample size calculation.

Clinicians should interpret this study with caution. The study does
not mean that acid suppression should not be used in children with asthma
and gastro-oesophageal reflux disease. In absence of robust evidence
against use of acid suppression, it could be tried in any child with
difficult to control asthma associated with gastro-oesophageal reflux
disease, along with other medical measures.

We read with interest the paper by Edge and colleagues[1] on
paediatric diabetes services in the UK which reports on data received from
169/216 (78%) of hospitals identified as delivering care to children with
diabetes. It reported that 95% of these clinics had registers of their
diabetic children (an improvement on previous years) and 75% of those
clinics held the data electronically. In a survey (Sep...

We read with interest the paper by Edge and colleagues[1] on
paediatric diabetes services in the UK which reports on data received from
169/216 (78%) of hospitals identified as delivering care to children with
diabetes. It reported that 95% of these clinics had registers of their
diabetic children (an improvement on previous years) and 75% of those
clinics held the data electronically. In a survey (September 2005) of the
16 units within Yorkshire who contribute data to the population based
Yorkshire Register of Children and Young People with Diabetes[2] we found
that 8/16 (50%) of these units rely on paper based records for clinical
management. However, they are safe in the knowledge that basic diagnostic
and demographic data are available electronically for their patients from
the Register. The apparent improvement in ‘computerisation’ of patient
data in diabetes clinics may therefore be an overestimate.

The National Diabetes Audit (NDA) of diabetes in England was recently
established under the direction of the Health and Social Care Information
Centre[3] and replaced the audit of children and adolescents with
diabetes in the United Kingdom previously undertaken by Diabetes UK (DUK).
It provides a key means to give healthcare workers information about the
quality of diabetes services and helps them monitor progress towards
meeting the Diabetes National Service Framework requirements.[4] For
their first report the NDA received data from 28 paediatric units. Both
the paper by Edge et al.[1] and our Yorkshire survey show that a
surprisingly large number of paediatric units have yet to implement
electronic systems. It seems that this failure to implement electronic
systems is caused by a combination of constraints arising from hospital
IM&T strategies requiring new systems to be compatible and share key
information with existing systems, lack of resource to implement new
systems and the low priority afforded for paediatric as opposed to adult
systems

When the National Audit was undertaken by DUK, data could be
submitted using not only electronic systems but in virtually any other
format (e.g. paper records) and resulted in submission of more than four
times the amount of data submitted to the NDA. However, not only does
this often entail double entry of data into these records (thus increasing
the likelihood of errors), but these methods are now inappropriate for
confidentiality reasons. The fact that the NDA relies on electronic
submission of data via NHSnet, coupled with the inability of many units to
collect or submit in this medium, may explain the relatively low
proportion of paediatric units participating so far. It is essential that
as many data as possible are submitted in order to draw meaningful
conclusions. The NDA are fully aware of these difficulties and are
working towards further guidance and assistance with the collection of
audit data, which is crucial for clinical governance, in units without
electronic systems.

Fiona M CampbellJeremy AllgroveJo DaltonPatricia A McKinneyOn
behalf of the National Diabetes Audit Paediatric User Group

FAO: Sherriff et al: I am not clear on what criteria you ranked
hygiene score. What is equivalent to hygiene score
0,1,2,...,11+? Could you please explain more for me? In addition, could you please send me the model of questionairre
base survey. I am looking forwards to hearing from you.

The conclusion to our study[1] was that there is little to be gained
by continuing the current screening of school children at 11 years for
colour vision defects. In his response, Dr Henderson agrees that the
current screening does not take into account the variability of both the
genotype and phenotype of the condition and that advising all affected
children similarly is overly simplistic and ineffe...

The conclusion to our study[1] was that there is little to be gained
by continuing the current screening of school children at 11 years for
colour vision defects. In his response, Dr Henderson agrees that the
current screening does not take into account the variability of both the
genotype and phenotype of the condition and that advising all affected
children similarly is overly simplistic and ineffective.

In our conclusion we suggest that other ways to inform young people
about potential occupational difficulties and pathways for referral for
specialist assessment would be more useful. This would indeed be an
improved and personalised approach to career advice which would allow for
assessment of those planning careers in occupations where colour vision is
essential and support for those affected by colour vision defects.

We previously assessed the impact of colour vision defects on
educational outcomes and found, at a population level, no difference in
outcome between those with colour vision defects and those with normal
colour vision.[2] It is of course possible that there may be some
children, with no family history of colour vision defects or other
indicator of potential difficulty, who are not being identified and helped
but this is not the rationale of the present screening programme. Our
study was carried out to inform the debate on the current screening
practice in the UK.

We read with great interest the article by D Singh-Grewal et al.[1] regarding the value of circumcision for the prevention of recurrent UTIs
in boys.

The article presents a reasonable case for considering circumcision
in some boys with recurrent UTIs.

However, we would like to bring to the authors’/readers’ attention
that both the original article and the quoted papers[2] make no mention
that chronic constipation is a risk factor for recurrent UTIs in
childhood.

Chronic constipation is a well-recognised and common risk factor in
children with recurrent UTIs. There is good evidence supporting this
relationship.[3]

Recognition and successful treatment of chronic constipation plays an
important role in the management of children with recurrent UTIs.

A study of this relationship by Vera Loening-Baucke in 1997 concluded
that “relief of constipation resulted in the disappearance of recurrent
urinary tract infections in all patients who had no anatomical abnormality
of the urinary tract.”[3]

This cause and effect relationship is supported by numerous other
studies going back to the 1970s.[4-7]

A recurring theme is that often the relationship between recurrent
UTIs and chronic constipation is not considered by either health care
professionals or the children’s carers.

Hence, it should not be forgotten that in children with recurrent
UTIs, chronic constipation is a major risk factor and should therefore be
considered in all cases.

Wall et al. treated infants with alleged iron deficiency anemia with
several iron vehicles. However, anemia in hospitalized ill infants is
mostly not due to iron deficiency, but to anemia of infection, present
even with mild infections. That's why they find a paradoxical decrease of
serum ferritin that rises with infection to fall after convalescence.
Anemia and all other measures of iron infection no...

Wall et al. treated infants with alleged iron deficiency anemia with
several iron vehicles. However, anemia in hospitalized ill infants is
mostly not due to iron deficiency, but to anemia of infection, present
even with mild infections. That's why they find a paradoxical decrease of
serum ferritin that rises with infection to fall after convalescence.
Anemia and all other measures of iron infection normalize without
therapy.[1] Thus, these results cannot be attributed to treatment. C
reactive protein is not completely reliable.